A rise in transvascular pulmonary fluid transport can be attributed to either an increase in the permeability of the exchange barrier or to a rise in the overall plasma to interstitial fluid driving force. I wish to investigate the effects of altering only the driving force on net fluid movement in the lung. The experimental phase of the investigation will include tracer estimates of capillary permeability and extravascular lung volume, the measurement of intravascular pressure, plasma and lymph osmolarity, the concentrations of eight plasma and lymph protein fractions and lung lymph flow in response to a change in transvascular pressure or osmolarity. Sheep will be used as the experimental animals. In the theoretical phase of the study a mathematical model, based on an equivalent pore analog of the capillary membrane, will be applied to the data. The model-predicted interstitial water volume and lymph protein fraction concentrations will be compared with the measured values throughout the transient period. If agreement with experimental data is good, then the model will be used to predict conditions which may lead to lung edema and, in addition, can be used to predict the rate at which water accumulates in the lungs. Even if the model is found to be inaccurate the data will be of valuable assistance in estimating optimal fluid therapy for patients at risk for pulmonary edema.